Persistent shoulder pain after stroke

Shoulder pain is a common complication after stroke, but its etiology is poorly understood. Treatment is generally unsatisfactory and chronic pain is common. This thesis adopts a mechanism-based approach to the research of PSSP development. The primary objective of the thesis is to obtain a better understanding of the pathophysiological mechanisms responsible for the development of persistent PSSP (pPSSP). Chapter 2 introduces the terminology and the neurophysiological concepts of pain and describes the theoretical framework that is used in the subsequent chapters. Subsequently, 3 cross-sectional studies are described that assessed chronic stroke patients with pPSSP by using pain research tools such as quantitative sensory testing and conditioned pain modulation (Chapter 3), cortical evoked potentials (Chapter 4), and the neuropathic pain diagnostic questionnaire (Chapter 5). The last part of the thesis focuses on the longitudinal assessment of pPSSP within 2 weeks, at 3 months and at 6 months after stroke. Chapter 6 describes the assessment of the complete clinical picture of somatosensory, motor, cognitive, emotional and autonomic functions in patient developing pPSSP. In chapter 7 the relationship between pPSSP and somatosensory loss, somatosensory sensitization and endogenous pain inhibition is studied. In summary, pPSSP was associated with both somatosensory loss and somatosensory sensitization as well as with altered central somatosensory processing. Moreover, in the chronic phase after stroke many patients with pPSSP reported neuropathic-like pain complaints. The influence of the presumed initiating factors may gradually decrease during the persistence of PSSP. Pain perpetuation may be related to a vicious circle of pain, limited range of motion, re-injury and somatosensory sensitization which may establish quite rapidly (i.e. within 3 months after PSSP onset) and may persist into the chronic phase after stroke. These studies confirm the multi-factorial etiology of pPSSP. Ongoing nociception, the brain lesion itself, and other (premorbid) factors may contribute to the development of pPSSP. Although the precise neurophysiological mechanisms still remain unclear, these findings have important implications for the assessment, prevention and treatment of PSSP.